Biomedical subjects

Matthias Brüwer

Publications and source records attributed to Matthias Brüwer.

3 recordsLinked to original sources

PubMed2006

Tight junctions and cell-cell interactions.

Chronic inflammation in mucosal tissues can influence epithelial barrier function via pro-inflammatory cytokines such as interferon (IFN)-gamma and tumor necrosis factor-alpha. Increased mucosal levels of these cytokines have been observed in mucosal biopsies from patients with a chronic inflammatory condition referred to as inflammatory bowel disease. Paracellular permeability across epithelial cells is regulated by tight junctions (TJs), which are the apical most junctions in epithelial cells. Given that pro-inflammatory cytokines modulate the epithelial barrier and that TJs regulate epithelial permeability, we analyzed the influence of IFN-gamma on U function/structure. Our results suggest that IFN-gamma induced a time-dependent increase in paracellular permeability that was associated with internalization of TJ transmembrane proteins, occludin, junction adhesion molecule A, and claudin-1. In this chapter, we focus on selected methods used to investigate the influence of IFN-gamma on epithelial barrier function.

Animals↗

PubMed2005

Ischaemic colitis mimicking inflammatory bowel disease in a young adult receiving oral anticoagulation.

Ischaemic colitis (IC) is the most frequent form of gastrointestinal ischaemia. Discrepancy between non-specific symptoms and objective findings is a hallmark of IC. Thus delay of diagnosis is common due to its often subtle and unpredictable presentation. In particular, the clinical symptoms and signs of IC can overlap with those of inflammatory bowel disease. We present a case of a young man with known factor-V-Leiden mutation in whom IC developed during effective therapy with oral anticoagulants, presenting with symptoms and endoscopic findings suggestive of inflammatory bowel disease.

Abdominal Pain↗

PubMed2002

Immunohistochemical expression of P53 and oncogenes in ulcerative colitis-associated colorectal carcinoma.

The role of the tumor suppressor gene p53 and proto-oncogenes mdm-2, waf-1,and bcl-2 in sporadic colorectal carcinoma (CRC) has been well investigated. However, little is known about the role of these genes in the development of ulcerative colitis-associated colorectal carcinoma (CAC). Colectomy specimens from patients with CAC, patients with ulcerative colitis (UC) and dysplasia, patients with long-standing UC without carcinoma or dysplasia, and patients with CRC were investigated in comparison to normal colon (NC) specimens from patients with diverticulosis without histologic signs of inflammation. Immunohistochemistry was performed with antibodies against p53, mdm-2, waf-1, and bcl-2; and staining was evaluated semiquantitatively with an expression of more than 20% of tumor cell nuclei or epithelial cell nuclei in nontumor specimens considered "positive." Statistical analysis was performed using Fisher's exact test. In carcinomas, p53 was positive in 50% of CRC tissues and 60% of CAC tissues without statistical difference. Positive expression of p53 was found in most high-grade dysplasia but not in low-grade dysplasia (p < 0.01). Whereas mdm-2 and bcl-2 were only sporadically expressed, waf-1 was observed in most specimens, with a high prevalence in UC without carcinoma or dysplasia (11/15). NC specimens were always negative for all antibodies. Immunohistochemical expression of p53, mdm-2, waf-1, and bcl-2 is similar for CAC and CRC. The malignant potential of dysplasia in UC is partially confirmed by a high prevalence of p53 and waf-1 expression, suggesting that CAC may develop along pathways that are different from CRC. High expression of waf-1 in nonmalignant long-standing UC has to be proved over a long-term course in its role as an independent cancer risk factor in UC patients.

Adult↗